Aim Toinvestigatetheroleofhyperglyce-mia in cerebral ischemia/reperfusion(I/R)injury with a middle cerebral artery occlusion(MCAO)rat model anditsmechanism.Methods EightyhealthymaleSD rats were randomly assigned into sham group, I/R group (normoglycemia),hyperglycemic I/R groupⅠ(HG1 )and hyperglycemic I/R groupⅡ(HG2 ).The cerebral I/R model was established by occluding the middle cerebral artery(MCA)in rats.Hyperglycemia was induced by intraperitoneal injection of 50% glu-cose solution.Neurological deficit was determined by Ludmila Belayev test;infarct size and brain edema were measured by TTC staining;mitophagy was ob-served by double immunofluorescent staining and elec-tron microscope.The expressions of autophagy-related proteins(LC3 and Beclin-1 )and apoptosis-related pro-teins(Cyt-C,AIF,caspase-9 and caspase-3 )were ex-aminedbyWesternblotfurtherly.Results Bloodglu-cose level was controlled at 4 mmol·L-1 (normoglyce-mia),10 mmol · L-1 (HG1 ) and 20 mmol · L-1 (HG2)respectively.There were no significant differ-ences between model group and HG1 group in neuro-logical deficit scores,infarct volume and edema size(P>0. 05 ).However,these indications in HG2 group were significantly increased compared with model group (P<0. 05 ).After 3 days of reperfusion,the level of mitophagy was significantly reduced accompanied with increased mitochondria damages in HG 2 group (P <0. 05 ),and the expressions of mitochondrial related ap-optotic proteins(Cyt-C,AIF,caspase-9 and caspase-3 ) were significantly increased accordingly compared to modelgroup.Conclusions Mildhyperglycemiacan not intensify the cerebal ischemic injury.In contrast, severe hyperglycemia significantly aggravates the brain ischemic injury by inhibiting the removal of injured mi-tochondria in a manner of mitophagy,thus amplifying the mitochondrial mediated cascade damage responses.

China ; Metals, Heavy ; Research Support as Topic ; statistics & numerical data

Objective To investigate the abnormality of fluid distribution and its effect on blood pressure (BP) in hemodialysis patients. Methods One hundred and six healthy volunteers as normal controls were divided into two groups(male group and female group).ECV%?ICV%(% means a percentage of weight) and ECV/ICV were measured by bioelectrical impedance spectroscopy and calculated in 2 groups respectively.Sixty-seven stable HD patients who had been on HD for more than 2 months in our hospital were selected. Patients were divided into 4 groups (hypotension prone group, normotensive group, hypertensive group and refractory hypertensive group). ECV%, ICV% and ECV/ICV were measured and calculated as above immediately before and after HD session. The measurement was conducted by Xitron 4200 HYDRA ECF/ICF Bio-Impedance Spectrum Analyzer. Results In patients on HD, a significant decrease of ECV% and ECV/ICV, and a significant increase of ICV% were seen post-HD. The pre-HD ECV% and ECV/ICV were significantly higher than those of normal controls but dropped close to normal level after hemodialysis. Post-HD ECV% was still higher than that of normal controls[(31.6?1.0)% vs (25.3?1.6)%, P 0.05]and post-HD ECV% of these patients was significantly lower than that of normal controlsand post-HD ECV% of these patients was significantly lower than that of normal controls[(19.3?1.6)% vs (22.6?1.4)%,P

70% were treated with stents.Patients were followed at 1 month and then every 3 to 6 months.Blood pressure and serum creatinine were measured and dosage of antihypertensive drugs were recorded.The Chinese equation was used to calculate estimated GFR.Results The mean follow-up period was 33.8?10.5(24-54) months.(1) Compared with baseline,blood pressure decreased siginificantly at 1 month and gained a further decrease at 24 months(SBP 129.1?12.9 mmHg vs 139.2?17.5 mmHg;DBP 72.6?7.1 mmHg vs 80.6?12.8 mmHg,both P0.05).Renal function was improved in 9.3% and stabilized in 62.9% of patients,and the overall benefit rate was 72.2%.(3) Logistic analysis revealed that male and diabetes were independent risk factors for renal function deterioration(OR=11.1 and 5.88,respectively,both P

Objective To evaluate the acute effects of different calcium concentration dialysate (1.25 mmol/L, 1.5 mmol/L, 1.75 mmol/L) on calcium balance and intact parathyroid hormone(iPTH) in maintenance hemodialysis(MHD) patients with normal serum tCa, and to provide scientific basis for individualized calcium concentration dialysate formula. Methods Dialysate with different calcium concentration (DCa1.25, DCa1.5, DCa1.75) was used in twelve stable MHD patients. Serum tCa, iCa(normalized to pH 7.4) and iPTH were assessed before and after each dialysis session with different calcium concentration dialysate. The iCa from fresh dialysate, spent dialysate at every 30 minutes interval and final total mixed spent dialysate were examined respectively. Phosphorus removal was also determined. Arterial blood pressure(BP) was measured every 30 minutes during hemodialysis session. Results With the DCa1.25, mean calcium loss was 5.03 mmol, but no significant changes of serum iCa and tCa between pre dialysis and post dialysis were found. Serum iPTH increased from (127.17?89.22)pg/ml to (281.92?244.84)pg/ml significantly (P

The suppressive effects of T. reglii on mouse cellular and humoral immune responses were studied. Lymphocyte proliferation effect induced with ConA,and PFC and OHS reactions with TD Ag(TNP-SRBC)were effectively suppressed by the drug. But the similar effects on LPS and TI Ag (TNP-SRBC) have not been found. The results shown that target cells of T. reglii effects may be T lymphocytes and the drug may not have a direct effect on B cells. The drug also shown a suppressive effect on IL-2 production by mouse spleen cells. The phenomenon suggests that the suppressive effects of T. reglii on humoral immune response may be indirectly mediated through suppressing helper T cells.

0.05).Conclusion Renal angioplasty showed a drug-dosage-saving effect on blood pressure and seemed to protect the renal function from deterioration in asymptomatic ARAS patients with stenosis ranged from 50% to 70%.Large-scaled and long-term studies are needed to verify our results.

OBJECTIVE: To explore the impact of of manganese (Mn) ions stress on the contents of cordycepin and adenosine in mycelia of C. militaris. METHODS: The mycelia biomass, Mn accumulation and activities of antioxidant enzymes [catalase (CAT), peroxidase (POD) and superoxide dismutase (SOD)] in mycelia of C. militaris with liquid culture medium supplemented with Mn from 0 to 100 g · L-1 were determined. The contents of cordycepin and adenosine in mycelia under different manganese oxidative stress were determined by HPLC. The separation was performed on a Zorbax Extend-C18 column (4.6 mm × 150 mm, 4 μm), using acetoni-trile-water (5:95) as the mobile phase. The flow rate was 1.0 mL · min-1. The detection wavelength was set at 254 nm. RESULTS: The mycelia biomass of C. militaris decreased with the increase of manganese concentration. The manganese content in mycelia increased significantly with the increase of manganese concentration and reached plateau when the manganese concentration was higher than 30 g · L-1. The activity of antioxidant enzymes including POD, CAT and SOD in mycelia of C. militaris all increased first and then decreased with increasing concentration of manganese in the culture media. The cordycepin content in mycelia increased significantly with increase of manganese concentration. When the Mn+ concentration in the culture medium was 80 g · L-1, cordycepin content in mycelia was 3.31 times higher than the control. The adenosine content decreased significantly when the manganese concentration was in the range of 0-30 g · L-1, and then remained relatively stable. CONCLUSION: Oxidative stress of manganese ions promotes the cordycepin synthesis in mycelia of C. militaris, but inhibites adenosine synthesis.

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China ; Foundations ; Preventive Medicine ; economics ; Research Support as Topic ; statistics & numerical data